The anatomophysiologic substrate of athetosis has heretofore resisted satisfactory explanation. Its most common concomitant from a neuropathologic point of view is striatal marbling but lesions may be placed in the striatum without evoking the phenomenon. Large lesions produce hyperkinesis of a nonspecific type. It has been found that lesions restricted to the rostral part of the striatum are especially potent in this respect. These lesions include the nucleus accumbens and the rostral extent of the nigrostriatal fibers. Current research is designed to investigate the possibility that the designated hyperkinesis may be evoked by involvement of that system alone.